Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1965 Oct;90(4):1001-6.
doi: 10.1128/jb.90.4.1001-1006.1965.

Endotoxin-induced susceptibility to staphylococcal infection and its reversal by adrenergic blocking agents

Endotoxin-induced susceptibility to staphylococcal infection and its reversal by adrenergic blocking agents

B M Sultzer et al. J Bacteriol. 1965 Oct.

Abstract

Sultzer, Barnet M. (Princeton Laboratories, Inc., Princeton, N.J.), and Henry H. Freedman. Endotoxin-induced susceptibility to staphylococcal infection and its reversal by adrenergic blocking agents. J. Bacteriol. 90:1001-1006. 1965.-The transient phase of increased susceptibility to bacterial infection in mice provoked by prior administration of small doses of endotoxin was investigated for possible mediation by vasoactive substances. Animals were given endotoxin intravenously shortly before intraperitoneal injection of Staphylococcus aureus Smith, thereby lowering the lethal inoculum 10-fold. To determine whether this susceptibility state could be obviated, mice were pretreated with phenoxybenzamine or dibenzylchlorethylamine. Mortality decreased from an average of 81% in the endotoxin control groups to about 23% in the treated mice, closely approximating the mortality in control mice injected with saline and staphylococci. Neither antiadrenergic agent independently altered the resistance of mice to a higher lethal staphylococcal challenge, nor did these materials induce extravascular leukocyte mobilization into the peritoneal cavity. The results suggest a possible role of vasoactive staphylococcal alpha-toxin, as well as epinephrine or epinephrine-like factors, in this altered state of resistance to staphylococcal infection.

PubMed Disclaimer

References

    1. J Exp Med. 1956 Dec 1;104(6):865-80 - PubMed
    1. J Exp Med. 1956 Jul 1;104(1):53-65 - PubMed
    1. J Exp Med. 1961 Nov 1;114:593-604 - PubMed
    1. J Exp Med. 1959 Sep 1;110:407-18 - PubMed
    1. J Exp Med. 1961 May 1;113:845-60 - PubMed

LinkOut - more resources